Mongolian gerbils subjected to unilateral cerebral ischemia showed an increased vesicular transport of peroxidase in the cerebral arterioles, venules and capillaries in the affected cerebral hemisphere. The amount of transferred peroxidase across the microvessels increased with duration of cerebral blood supply deprivation, which never resulted in degeneration of the endothelial cells in the brain vessels. The intercellular spaces between the endothelial cells were free of peroxidase from the lumen to the first abluminal tight junction.